Peracetic acid

Endpoint summary

Description of key information

Systemic bioavailability of peracetic acid is not expected due to its rapid degradation upon contact with skin and/or saliva and their containing catalases.

Key value for chemical safety assessment

Bioaccumulation potential:

no bioaccumulation potential

Additional information

In order to investigate the overall metabolic fate of acetic acid and peracetic acid following a single dermal application rats were treated in accordance with OECD guideline 417 with radio labelled Proxitane 0510 containing 5 % peracetic acid (Phillips, 1994). One group of four male rats was given a single application of 14C-labelled Proxitane 0510 to an enclosed area (approx. 4.5 cm2) of clipped dorsal skin. This treatment should reflect the conditions of the maximum concentration that an individual is likely to be exposed to and allow the determination of any significant accumulation of the test substances in tissues. The treated animals were placed in metabolism cages and respired air, urine and faeces were analysed for radioactivity content up to 72 hours post-treatment. Animals were then killed and the radioactivity in the treated skin, major organs and remaining carcass determined. A second group of four rats was given a single application of 14C-labelled acetic acid/hydrogen peroxide solution to act as a control group. The fate of the radioactivity was compared with that from the 14C-labelled Proxitane 0510-treated animals and the percentage of radioactivity found in treated skin, major organs, remaining carcass as well as in respired air, urine and faeces was determined up to 72 hours post-treatment.

Following topical application onto the skin of male rats, only a small portion of the administered dose (< 1%) was recovered as unchanged acetic acid or peracetic acid while approximately 30 – 60% of the dose was recovered as CO2 (mean of about 58% in the Proxitane group vs. a mean of about 37% in the acetic acid group). In the case of radio labelled Proxitane, formation of CO2 occurred after an initial lag phase of approx. 1 hour. It is possible that this initial lag phase is due to a lower blood flow in skin capillaries and a slower distribution due to micro-emboli resulting from oxygen formation after contact and damage to the skin.

Virtually no volatilisation from treated skin was observable in the Proxitane-treated group. The excretion via the faeces was comparable between the two materials (about 4 - 5% of given radioactivity), while the percentage of tissue-bound radioactivity was higher after administration of Proxitane (mean of about 20% in the Proxitane group vs. a mean of about 10% in the acetic acid group) and urinary radioactivity was higher after administration of acetic acid (mean of about 17% in the Proxitane group vs. a mean of about 23% in the acetic acid group). In tissues, highest levels of radioactivity were found in liver, gastrointestinal tract and exposed skin. In the Proxitane group, severe skin damage was observable which was not evident in the acetic acid group. However, radioactivity found in the exposed skin was comparable between the Proxitane and the acetic acid group (approx. 0.2 – 0.4% of the dose applied). Overall recovery of topically applied radioactivity was 56 – 73% (mean of 61 %) in the Proxitane-treated group and 69 – 83% (mean of 73%) in the acetic acid-treated group. It was concluded that due to its high reactivity and rapid degradation, peracetic acid is not expected to enter the body and become systemically available after dermal application. The absence of a systemic bioavailability of peracetic acid is confirmed by its rapid degradation upon contact with skin due to skin damage. In addition, it could be observed in this study that the kinetic behaviour and also the percentage of absorbed and excreted radioactivity as well as the radioactivity found in different organs is comparable after topical administration of peracetic acid (given as Proxitane 0510) and acetic acid, respectively. The latter observation suggests, that the chemical entity entering the body after dermal application will be restricted to acetic acid only which is in accordance with the high reactivity and degradation of peracetic acid.

The fate of peracetic acid in blood was investigated in vitro (Van Egdom, 2005). In a first experiment blood samples were taken from a male Wistar rat and 1000 times diluted with peracetic acid test solutions of different concentrations (1.0 and 5.0 mg/L) in physiological saline. A test solution without blood was implemented as a control. The solutions were incubated at 37°C and samples were taken immediately after addition and at 5, 15, 30, 60, 120 and 240 minutes. Peracetic acid oxidises MTS (methyl-p-tolylsulfide), which was added to each of the samples. The resulting MTSO (methyl-p-tolylsulfoxide) was monitored by HPLC, the concentration of peracetic acid was calculated. After 5 minutes which is needed for sample preparation until analysis, less than 0.1 mg/L peracetic acid was present in both solutions. Hence, the half-life of peracetic acid in rat blood is less than 5 minutes. The concurrent control solution containing no blood showed a much slower degradation: after 5 minutes only few peracetic acid had degraded and the half-life in this case was about 4 hours

In a second study blood samples from a male Wistar rat were also diluted 1000 times with solutions of the test item Peraclean 15 containing 15.22% (w/w) peracetic acid and 14.27% (w/w) hydrogen peroxide in different concentrations (DeGroot, 2003). These doses correspond to 0, 5.4, 10.8, 21.6 mg/L and of H2O2 of 0, 5.1, 10.1, 20.3 mg peracetic acid/L, respectively). Samples were taken immediately before and after addition of blood, at 5, 15, 30, 60, 120, 240 minutes and after 24 hours. When solutions of the test item with concentrations of 10 mg/L or less are mixed with 1000 times diluted rat blood, rapid degradation of peracetic acid and hydrogen peroxide occurs. The half-lives are well below 5 minutes. At a concentration of 21.6 mg/L and 20.3 mg/L for peracetic acid and hydrogen peroxide, respectively, there is an initial strong decrease of the concentration which afterwards flattens and decreases more slowly.

Both experiments demonstrate that peracetic acid and hydrogen peroxide degrade rapidly in rat blood.

In view of the use of peracetic acid containing products for the disinfection of stables, the cutaneous tolerability and penetration of peracetic acid following topical application of diluted peracetic acid alone and a diluted Wofasteril solution (application concentration in both cases 1.5 % peracetic acid) was investigated in a subchronic 120-day study in a total of 19 pigs (Krüger and Jancke, 1976). Pigs (initial weight approx. 33 kg) were treated with a dose of 250 mL/animal/day corresponding to a daily dose of about 114 mg/kg bw/d. After termination of the study, residues of the test item were analysed in muscles, liver and adipose tissue. In an accompanying model trial the penetration of peracetic acid through treated and untreated skin was investigated.

The slaughter samples taken demonstrated neither histological nor organoleptic changes in the test and control groups. There was no influence on pH and colour brightness of the meat following topical treatment with peracetic acid and Wofasteril demonstrating no effect of peracetic acid on meat quality. Analysis of muscles, liver and adipose tissue on residues of peracetic acid and its metabolite hydrogen peroxide were negative by the methods used. No adverse effects on meat quality and no detectable residues of peracetic acid and/or its metabolite hydrogen peroxide were observed in muscles, liver and adipose tissue, respectively. The results lead to the conclusion that peracetic acid and hydrogen peroxide either did not penetrate pig skin in vivo or degraded so rapidly as to result in non-detection in these organs/tissues. The results of the diffusion trials of peracetic acid through treated and untreated pig skin in vitro demonstrated that no penetration of peracetic acid through pig skin was found through intact skin while absorption of peracetic acid through damaged skin cannot be entirely excluded.

Overall it can be concluded, that peracetic acid is degraded by catalases found in blood, stomach fluid, saliva as well as in various organs. Most importantly, degradation by catalases in human erythrocytes was demonstrated. The absence of systemic bioavailability of peracetic acid is confirmed by its rapid degradation upon contact with skin resulting in the observed skin damage as well as by the observation of the non-enzymatic degradation to acetic acid and oxygen at pH values of around 7 which is close to physiological pH values in blood and in cells, respectively.